C-FOS-LIKE IMMUNOREACTIVITY IN THE SUBFORNICAL ORGAN AND NUCLEUS OF THE SOLITARY TRACT FOLLOWING SALT INTAKE BY SODIUM-DEPLETED RATS

Citation
Ta. Houpt et al., C-FOS-LIKE IMMUNOREACTIVITY IN THE SUBFORNICAL ORGAN AND NUCLEUS OF THE SOLITARY TRACT FOLLOWING SALT INTAKE BY SODIUM-DEPLETED RATS, Physiology & behavior, 63(4), 1998, pp. 505-510
Citations number
33
Categorie Soggetti
Psychology, Biological","Behavioral Sciences
Journal title
ISSN journal
00319384
Volume
63
Issue
4
Year of publication
1998
Pages
505 - 510
Database
ISI
SICI code
0031-9384(1998)63:4<505:CIITSO>2.0.ZU;2-4
Abstract
Acute sodium depletion by furosemide induces a robust salt appetite in the rat which is satiated rapidly by ingestion of sodium chloride (sa lt) solutions. To identify neuronal populations activated by sodium de pletion and by salt intake, we quantified c-fos-like immunoreactivity (c-FLI) in the subfornical organ (SFO) and nucleus of the solitary tra ct (NTS) after sodium depletion and at time intervals from 30 min to 1 2 h after 1 h of access to 0.3 M NaCl. Rats drank 10 +/- 1.6 mt over 1 h, with most of the intake occurring by 30 min. Increased numbers of c-FLI-positive cells were observed in the SFO 24 h after sodium deplet ion; c-FLI remained,elevated for 90 min after 0.3 M NaCl intake and th en declined until the number of c-FLI-positive cells at 12 h was not s ignificantly different from mock-depleted levels. Sodium depletion alo ne did not significantly elevate c-FLI in the NTS, bur the number of c -FLI-positive nuclei in the NTS was significantly increased after 0.3 M NaCl intake. The cellular location and temporal pattern of c-FLI exp ression are consistent with activation of neural circuitry sensitive t o humoral, gustatory, and postingestive stimuli accompanying sodium de pletion and 0.3 M NaCl ingestion. c-FLI in the SFO and NTS may serve a s quantifiable markers in the central nervous system of the state of s odium depletion and of ingestive (orosensory and gastrointestinal) sen sory stimulation, respectively. (C) 1998 Elsevier Science Inc.